Glomerulus nephritis

Introduction to glomerulonephritis Glomerulonephritis is also known as nephritis. An allergic disease that occurs in bilateral renal glomeruli. Glomerulonephritis is a common kidney disease, divided into acute and chronic. Acute nephritis has an acute onset and a short course of disease. It occurs in children aged 4 to 14 years, and more men than women. Most of the disease occurred after streptococcal infection. Most cases had pre-infections such as pharyngitis and tonsillitis 2 to 3 weeks ago, but there was no parallel relationship between the degree of infection and whether or not the disease occurred. basic knowledge The proportion of illness: 0.03% Susceptible people: no special people Mode of infection: non-infectious Complications: anemia, high blood pressure

Causes of glomerulonephritis

Whether nephritis is a hereditary nephritis will not be related to what kind of nephritis. Some nephritis is hereditary, especially hereditary nephritis, which can be inherited by parents to children. It is an autosomal dominant genetic disease that can be passed on to future generations.

The cause of nephritis is unclear in the medical community and is generally thought to be caused by a genetic defect in the synthesis of glomerular basement membrane. This disease has a characteristic, that is, there is a clear family history, often in a family of several generations of family, many people have hematuria, hematuria is the most common manifestation of hereditary nephritis, more common in young men.

When the onset of nephritis is usually not obvious, children often have mild proteinuria and hematuria in urine, often after severe exercise or upper respiratory tract infection. Generally, proteinuria gradually increases with age, and individual cases may have severe proteinuria. Blood pressure is rarely increased, and it is often mildly elevated in the late stage. The condition progresses slowly and slowly, and the male condition is more serious. He often dies in chronic renal failure in his prime, and the woman is milder and has a normal life expectancy.

Streptococcal infection (30%):

Group A group B hemolytic streptococcus is the most important bacteria causing glomerulonephritis. After group A group B hemolytic streptococcus infection causes tonsillitis and scarlet fever, the antigen of sputum bacteria binds to antibodies (immunoglobulin) in human body. Forming an antigen-antibody immune complex, deposited on the glomerular basement membrane, can cause a series of inflammatory reactions.

Viral infection (20%):

After infection with influenza virus, measles virus, varicella virus, mumps virus, adenovirus, etc., although the incidence of acute glomerulonephritis is very low, the mechanism is still unclear, but if there is a history of viral infection in the clinic, there is no bacterial infection. Symptoms, urine changes lightly, when nephritis syndrome is not typical, should consider whether it is nephritis after viral infection.

Other (15%):

Syphilis, brucellosis, typhoid, typhus, protozoal infection, mold infection, etc., can also cause acute glomerulonephritis. Non-infectious diseases, such as foreign protein intake, drugs, tumors, systemic diseases such as lupus erythematosus, can also lead to acute glomerulonephritis.

Glomerulonephritis prevention

Work and rest

In daily work, whether it is physical or mental work, patients with nephritis should not be excessively tired, and should rest more, otherwise it will increase the abnormal metabolism, increase the burden of kidney function, and even damage the kidney.

2. Pay attention to the regulation of emotions

Patients with chronic nephritis must establish confidence in the fight against the disease, because the condition of chronic nephritis is slowly extended, so it is necessary to maintain the determination and confidence of treatment; temper, worry will cause liver damage, affect the disorder of the secretion system, and directly Damage to kidney function.

3. Pay attention to diet

Unreasonable diets tend to exacerbate the kidney burden of patients with chronic nephritis, leading to further damage to kidney function, leading to continued deterioration of the disease. According to the characteristics of chronic nephritis, patients should be asked to have a reasonable diet for kidney disease.

4. Couples should live regularly

For husband and wife life, patients with chronic nephritis should not be too frequent, generally not more than twice a month, if it exceeds, it will easily lead to relapse and deterioration of the disease.

5. Forbidden to take anti-inflammatory analgesics

For example, cold medicines and antibiotics must be taken under the guidance of relevant doctors before using anti-inflammatory analgesics, because improper use of these drugs directly damages kidney function, leading to abnormal kidney function.

Glomerulonephritis complications Complications, anemia, hypertension

1. Circulatory congestion: due to water and sodium retention, blood volume exhaustion, until pulmonary edema. The incidence rate varies from report to report, depending on the severity of the condition and treatment. In the 50s and 60s of our country, we reported such complications in 24% to 27% of children with acute nephritis. In recent years, the report has dropped to 2.4%. Most occur within 1 to 2 weeks after the onset of acute nephritis. The clinical manifestations are symptoms of shortness of breath, inability to supine, chest tightness, cough, wetness of the lungs, hypertensive liver, galloping, and other symptoms of heart failure, which are caused by the expansion of blood volume, and are different from true myocardial pumping. At this time, the cardiac output is often increased without decreasing, the circulation time is normal, the arteriovenous oxygen partial pressure difference is not increased, and the digitalis is not good, and the application of diuretics can often alleviate it. Very few severe cases can progress to true heart failure, and pulmonary edema rapidly becomes life-threatening within a few hours to 1-2 days.

2. Hypertensive encephalopathy: refers to a sharp increase in blood pressure (especially diastolic blood pressure), in the case of central nervous system symptoms. Children are more common than adults. It is generally believed that this disease is based on systemic hypertension. Intracerebral resistance, small vasospasm leads to cerebral hypoxic cerebral edema. However, it is also believed that when the blood pressure rises sharply, the cerebral vasculature has an automatic systolic and regurgitation function that is out of control. The cerebral blood vessels are highly congested and cerebral edema causes water and sodium retention in acute nephritis to play a role in the pathogenesis.

Occurred in the early stage of acute nephritis, the onset is generally more acute, manifested as severe headache, frequent nausea and vomiting, followed by visual impairment, vertigo, double vision, temporary darkness, and sleepiness or irritability, if not treated in time Convulsions, coma, a small number of temporary hemiplegia, and severe cerebral palsy. There are many limitations of the nervous system. Shallow reflexes and sacral reflexes can be weakened or disappeared. The sputum sputum is sometimes positive, and pathological reflex can also occur. In severe cases, there may be symptoms and signs of cerebral palsy. Fundus examination common retinal arteriolar spasm, sometimes visible optic nerve head edema. The cerebrospinal fluid is clear, and the pressure and protein are normal or slightly increased. If the blood pressure exceeds 18.7/12.0kpa (140/90mmhg), it can be diagnosed with one of visual impairment, convulsion and coma.

Glomerulonephritis symptoms Common symptoms Intermittent hematuria persistent urinary protein lower extremity edema hypertension no hematuria with proteinuria highly bloated capillary vasospasm facial edema less urinary hematuria

Prodromal symptoms

Most patients have a history of pioneer infection one month before the onset of the disease, and the onset is sudden, but it can also occur slowly and slowly.

Onset

Start with less urine, or gradually oliguria, or even no urine. Can be accompanied by gross hematuria, duration, but microscopic hematuria persists, urine changes are basically the same as acute glomerulonephritis.

Edema

About half of the patients developed edema at the beginning of oliguria, with the face and lower limbs as the weight. Once the edema appears, it is difficult to subside.

hypertension

Some patients are accompanied by high blood pressure at the onset of the disease, and there is also high blood pressure during the onset of the disease. Once the blood pressure is increased, it is persistent and not easy to decline on its own.

Renal impairment

A persistent increase is a feature of the disease. Significant reduction in glomerular filtration rate and renal tubular dysfunction.

The pathological change of glomerulonephritis is that the volume of the kidney can be increased more normally, and the lesion mainly involves the glomerulus. The pathological type is intravascular proliferative glomerulonephritis. Light microscopy is usually diffuse glomerular lesions, with endothelial cells and mesangial cell hyperplasia as the main manifestations, acute phase may be accompanied by neutrophil and mononuclear cell infiltration. When the lesion is severe, the hyperplastic and infiltrating cells can compress the capillaries, narrow the capillary lumen, or even occlude, and damage the glomerular filtration membrane, which may cause hematuria, proteinuria and tubular urine; and make the glomerulus The filtration rate is reduced, so the excretion of water and various solutes (including nitrogen metabolites, inorganic salts) is reduced, and sodium and water retention occurs, which in turn causes an increase in extracellular fluid volume. Therefore, there is clinical edema, oliguria, and systemic circulation. The state of congestion is difficult to breathe, the liver is large, and the venous pressure is increased. Renal tubular lesions are not obvious, but the renal interstitial may have edema and focal inflammatory cell infiltration.

Examination of glomerulonephritis

1, through urine protein qualitative, urine sediment microscopic examination, you can initially determine whether there is glomerular lesions.

2, urine routine examination: urine color is generally no abnormality, urine protein is generally not much, urinary sediment increased leukocytosis (acute period often full of vision, chronic phase in 5 / high power field), sometimes can produce white blood cell cast.

3, urine bacteria check: When the urine contains a large number of bacteria, due to urinary sediment coating for Gram stain test, about 90% can find bacteria. This method is simple and has a high positive rate.

4, urine cell count: in recent years, the use of 1 hour counting method, it is considered that the 12-hour urine sediment count is accurate and simple. The standard is that the number of white blood cells is more than 300,000 / hour is positive, less than 200,000 / hour can be considered as a normal range, between 200,000 and 300,000 / hour should be combined with clinical judgment; red blood cells greater than 100,000 / hour is positive.

Diagnosis and diagnosis of glomerulonephritis

Diagnostic criteria

1. Acute onset, hematuria, proteinuria, often with hypertension and edema, or with oliguria and azotemia, occasionally left heart failure, pulmonary edema or hypertensive encephalopathy.

2. On the basis of the above-mentioned acute nephritic syndrome, glomerulonephritis after acute streptococcal infection can be diagnosed if there are two points in the following points:

1. Detection of a strain of Streptococcus nephrii in a skin lesion or pharynx;

2. Positive for the immunoassay of streptococcus and enzymes;

3. Serum complement C3 temporarily decreased.

The main basis for the diagnosis of acute glomerulonephritis:

1. History of pre-infection: There are skin or respiratory infections before the onset of illness, and there may be infections in other parts;

2. manifested as hematuria, edema, oliguria, hypertension, urine routine urine with proteinuria, visible particles or transparent cast;

3. Serum complement decreased, ESR increased, with or without ASO elevation. Those with the above characteristics can be diagnosed, but should pay attention to the acute prostatitis caused by the virus may have a short prodromal period, usually 3 to 5 days, with hematuria as the main performance, C3 does not decrease, ASO (anti-streptolysin O) does not increase, The prognosis is good.

Differential diagnosis:

(1) acute exacerbation of chronic nephritis: most chronic nephritis, often insidious onset, acute attacks often secondary to acute infection, the prodromal period is often shorter, 1 to 2 days of edema, oliguria, [1] nitrogen Symptoms such as blood, serious cases can be accompanied by anemia, high blood pressure, poor renal function, usually with nocturia, urine specific gravity or fixed low specific gravity urine.

(2) Rapid progressive nephritis: It is difficult to identify acute onset of acute nephritis at the beginning of the disease; the progressive renal insufficiency can help identify the disease within a few weeks, and if necessary, renal pathological examination, such as crescentic nephritis can be identified.

(3) acute urinary tract infection: urinary routine can appear red blood cells, but often accompanied by white blood cells and pus cells, some patients have fever and urinary tract irritation, middle urine culture can be diagnosed, often complement normal.

(4) Membrane proliferative nephritis: often with acute nephritis onset, but often proteinuria is obvious, serum complement continues to decline (more than 8 weeks), the disease recovery is not as good as acute nephritis, if necessary, a renal biopsy to confirm the diagnosis.

(5) IgA nephropathy: mainly with recurrent hematuria as the main manifestation, ASO and C3 are often normal, and renal biopsy can confirm the diagnosis.

(6) secondary nephritis: such as sensitized purpura nephritis, lupus nephritis, hepatitis B virus-associated nephritis.

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